Publications by authors named "Zao Cheng Xu"

Article Synopsis
  • Excess glutamate release from presynaptic neurons is linked to ischemic neuronal death, with CA1 pyramidal neurons being more vulnerable than CA3 neurons, hinting at distinct properties of these cells contributing to this difference.
  • After ischemia, CA1 neurons showed increased dendritic spines and changes in glutamate receptor subunit expression, particularly a rise in the NR2B/NR2A ratio and a decrease in the GluR2 subunit.
  • In contrast, CA3 neurons remained relatively unchanged in synaptic density and receptor expression post-ischemia, suggesting that structural changes in CA1 neurons drive delayed cell death following ischemic events.
View Article and Find Full Text PDF

Animal models of cerebral ischemia have typically been established and performed using young animals, even though cerebral ischemia (CI) affects primarily elderly patients. This situation represents a discrepancy that complicates the translation of novel therapeutic strategies for CI. Models of transient global CI using aged animals have demonstrated an apparent neuroprotective effect on CA1 hippocampal neurons; however, this effect is not completely understood.

View Article and Find Full Text PDF

Descending propriospinal neurons (DPSN) are known to establish functional relays for supraspinal signals, and they display a greater growth response after injury than do the long projecting axons. However, their regenerative response is still deficient due to their failure to depart from growth supportive cellular transplants back into the host spinal cord, which contains numerous impediments to axon growth. Here we report the construction of a continuous growth-promoting pathway in adult rats, formed by grafted Schwann cells overexpressing glial cell line-derived neurotrophic factor (GDNF).

View Article and Find Full Text PDF

Striatum is one of the brain regions that are highly sensitive to transient cerebral ischemia. Most of the striatal neurons die shortly after ischemia but interneurons including large aspiny (LA) neurons survive the same insult. Previous studies have shown that inhibitory synaptic transmission is enhanced in LA neurons after ischemia.

View Article and Find Full Text PDF